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In vivo Injected Mitochondria-Targeted Plastoquinone Antioxidant SkQR1 Prevents β-Amyloid-Induced Decay of Long-Term Potentiation in Rat Hippocampal Slices

N. A. Kapay1*, N. K. Isaev1,2,3*, E. V. Stelmashook1,3, O. V. Popova1, D. B. Zorov2,3, V. G. Skrebitsky1, and V. P. Skulachev2,3

1Department of Brain Research, Research Center of Neurology, Russian Academy of Medical Sciences, Pereulok Obukha 5, 105064 Moscow, Russia; E-mail: kapayn@gmail.com

2Belozersky Institute of Physico-Chemical Biology, Lomonosov Moscow State University, 119991 Moscow, Russia; E-mail: isaev@genebee.msu.ru

3Institute of Mitoengineering, Lomonosov Moscow State University, 119991 Moscow, Russia; E-mail: info@skq-project.ru

* To whom correspondence should be addressed.

Received September 13, 2011; Revision received October 17, 2011
Addition of 200 nM β-amyloid 1-42 (Abeta) to a rat hippocampal slice impairs the induction of a long-term post-tetanic potentiation (LTP) of population spike (PS) in pyramidal neurons of the CA1 field of hippocampus. Intraperitoneal injection into the rat of the mitochondria-targeted plastoquinone derivative SkQR1 (1 µmol/kg of weight given 24 h before the slices were made) abolishes the deleterious effect of Abeta on LTP. These data demonstrate that SkQR1 therapy is able to compensate the Abeta-induced impairments of long-term synaptic plasticity in the hippocampus, which are the main cause of loss of memory and other cognitive functions associated with Alzheimer’s disease.
KEY WORDS: Alzheimer’s disease, β-amyloid, long-term memory, long-term potentiation, neurons, hippocampus, mitochondria-targeted antioxidants, SkQR1

DOI: 10.1134/S0006297911120108